Embolization of Tumors: Brain, Head, and Neck, and Spine

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Chapter 89 Embolization of Tumors

Brain, Head, Neck, and Spine

Hypervascular neoplasms of the central nervous system (CNS) can be formidable surgical challenges associated with significant morbidity and mortality. Vascular tumors can result in excessive intraoperative blood loss, prompting termination of the surgery before achieving its goals. Multiple reports have suggested preoperative embolization can reduce intraoperative blood loss, the need for transfusions, operative time, and the length of hospitalization.14 Embolization also may reduce mass effect and alleviate pain.5 Furthermore, preoperative embolization can facilitate a more complete surgical extirpation by clarifying the surgical field, enhancing tumor boundaries, and shrinking the tumor.

In most cases, preoperative embolization of arterial pedicles in various vascular CNS tumors is technically feasible, regardless of the tumor’s origin and location (Table 89-1). The goals of tumor embolization are sacrificing the feeding vessels and obliterating the tumor capillary bed to the greatest extent possible. These goals must be balanced against the risks of embolization, which include occlusion of en passage vessels, pulmonary emboli, retained microcatheters, and compression of eloquent neural tissues by expanding intratumoral edema or hemorrhage.

TABLE 89-1 Barrow Neurologic Institute Series of 169 Embolized CNS Tumors (1995-2009)

Tumors No.
 Olfactory groove 2
 Convexity 10
  Skull base 1
  Parasagittal 3
  Frontal 5
  Sphenoid 3
 Glomus jugulare 17
 Glomus tympanicum 1
 Carotid body tumors 7
Hemangioblastoma 12
Juvenile Nasal Angiofibroma 25
Hemangiopericytoma 3
 Plasmacytoma (spinal) 1
 Aneurysmal bone cyst (spinal) 2
 Thyroid carcinoma met (spinal) 1
 Hemangioma (skull base) 1
 Hemangioma (facial) 2
 Hemangioma (spinal) 4
 Renal carcinoma met (spinal) 12
 Renal carcinoma met (cranial) 1
 Giant cell tumor 3
 Vestibular schwannoma 1
 Jugular foramen nerve sheath tumor 1
 Synovial cell sarcoma (spinal) 1
 Osteogenic sarcoma (spinal) 1
 Schwannoma (spinal) 2
 Pharyngeal carcinoma 2
 Chordoma (spinal) 1
 Nasal polyp 1
 Thyroid carcinoma 1
 Melanoma (spinal) 1
 Dural cavernous malformation 1
Total 129

Tumors of the Head


Meningiomas originate from arachnoid cap cells and can be hypervascular. They are slightly more common in females than in males and account for 13% to 18% of all intracranial tumors.6 Typically, they are benign, with the potential for a surgical cure with complete resection. Recurrence rates are inversely proportional to the extent of surgical resection. Angiography and preoperative embolization of intracranial meningiomas are common practices used to improve the chances obtaining complete resection and a cure. The resection of many large meningiomas has been aborted due to heavy intraoperative blood loss, a complication that can be mitigated with judicious use of preoperative embolization. Angiography can also assist surgical planning by delineating the vascular supply to the tumor, the encasement and patency of vascular structures (arteries or dural venous sinuses), the degree of displacement of neuronal elements, and the site of dural attachment.

The blood supply to meningiomas is typically twofold: large arterial pedicles and pial and cortical arteries. Classically, large arteries supply the site of dural attachment and the center of the tumor, creating a “sunburst” appearance on angiography. The apex of the sunburst is usually the site of dural attachment. The pial and cortical vessels usually supply the tumor capsule, with their vascular contribution increasing as the tumor enlarges. Large arterial pedicles typically arise from branches of the external carotid artery (ECA), but they may also arise from the internal carotid artery (ICA). Dural pedicles arising from the ECA include the middle meningeal artery (MMA), accessory meningeal artery, neuromeningeal artery (arising from the ascending pharyngeal artery), and stylomastoid artery (arising from the occipital artery). The ICA occasionally supplies meningiomas via ethmoidal, cavernous, clival, or tentorial branches.

The location of the meningioma suggests which vessels warrant scrutiny during angiography. Anterior fossa meningiomas can be supplied by both the ICA and the ECA. Diaphragmatic or tuberculum sellae meningiomas frequently derive the majority of their blood supply from the ICA. High-convexity and parasagittal tumors tend to feed from the MMA, superficial temporal artery (STA), and artery of the falx cerebri and warrant angiography of the bilateral anterior circulation. Tumors of the anterior falx or frontal convexity frequently receive their blood supply from the meningeal branches of the ethmoidal artery and anterior falcine branches or, occasionally, from the anterior cerebral artery or a tentorial branch of the ophthalmic artery. Bilaterally, the anterior or posterior ethmoidal arteries often supply olfactory groove lesions, and evaluation of the ophthalmic and distal internal maxillary arteries must be meticulous.

Branches of the ECA, specifically the artery of the foramen rotundum, vidian arteries, or accessory meningeal artery, often supply middle fossa meningiomas. The vascular supply of meningiomas involving the sphenoid wing often derives from the recurrent meningeal branch of the ophthalmic artery or from branches of the MMA. Parasellar meningiomas tend to be fed by branches of the petrous, cavernous, or supraclinoid branches of the ICA; the artery of the foramen rotundum; the artery of the foramen ovale; or the neuromeningeal branch of the ascending pharyngeal artery.

The vascular supply of posterior fossa meningiomas is usually from the posterior meningeal artery, MMA, or accessory meningeal artery. Classically, tentorial meningiomas receive arterial feeders from the tentorial branch of the meningohypophyseal trunk (MHT), but they can be supplied by the infratentorial trunk, MMA, or accessory meningeal artery. Petroclival lesions are often supplied by the MMA (frequently from the petrosal, petrosquamosal, or occipital branches), transmastoid branches of the posterior auricular or occipital arteries, anterior inferior cerebellar artery (AICA, via the subarcuate branch), or neuromeningeal branch of the ascending pharyngeal artery.

The common vascular origins shared by posterior fossa meningiomas and cranial nerves require diligent attention when embolization of these lesions is considered. For example, cranial nerves III to VI share blood supply with tentorial meningiomas via the MMA, MHT, or accessory meningeal artery branches. Provocative testing before embolization can minimize the risks of inadvertently injuring the cranial nerves. Furthermore, extracranial-to-intracranial (EC-to-IC) arterial anastomoses, particularly between posterior auricular or occipital arteries and the high cervical spinolaminar segment of the vertebral artery (VA), may be present.

Meningiomas commonly invade the dural venous sinuses. Patency of the adjacent sinus and surrounding cortical veins is an important consideration and should be evaluated to facilitate surgical planning. Complete occlusion of the venous sinus may allow aggressive surgical resection through excision of the involved portion of the sinus.


Many meningiomas do not require preoperative embolization because they often can be easily devascularized at surgery. At our institution, we recommend preoperative embolization of giant meningiomas, meningiomas involving the middle cranial fossa or skull base, falcine or parasagittal meningiomas, or meningiomas of the pineal region (Fig. 89-1). During surgery, the vascular supply to skull base meningiomas is frequently obscured until a substantial portion of the tumor has been excised, emphasizing the beneficial utility of embolization in these cases. In patients who are poor surgical candidates, embolization may be offered as a palliative measure to slow tumor growth.

Large, hypervascular skull base tumors whose vascular supply is not readily accessible via surgery should be evaluated for preoperative embolization. Embolization of deep-feeding arteries such as the inferolateral trunk and MHT can be technically challenging due to their small caliber and acute angle of origin. Technological advances in microcatheters and microguidewires have facilitated superselective catheterization of these blood vessels and expanded the range of treatable intracranial lesions through embolization. Even so, the potential for reflux of embolic material into the ICA remains a serious concern, and these lesions continue to present major challenges for even the most experienced neurointerventionalists. Abdel Kerim et al. described a technique of inflating a balloon in the MHT distal to the exit of a tumoral feeding artery to improve the penetration of Onyx (ev3 Endovascular, Irvine, CA) into the feeding vessel.7 Several authors have successfully embolized middle fossa tumors with deep-feeding arteries with good surgical and radiographic outcomes.810 The inferolateral trunk occasionally has collaterals with the ophthalmic artery via the deep recurrent ophthalmic artery. During embolization of the inferolateral trunk, extreme caution is warranted to minimize the risk of potential blindness.

Embolization of pial or ophthalmic branches is usually considered too perilous to undertake. However, Kaji et al. reported two cases in which distal cortical ICA branches were successfully embolized with Gelfoam (Pharmacia & Upjohn Company LLC, Peapack, NJ) before surgery.11 Based on their experience, these authors recommend that embolization of pial or cortical vessels only be undertaken if the following conditions are met: (1) The tumor is supplied exclusively by the ICA. (2) The tumor is located in a noneloquent portion of the brain. (3) The patient has a negative sodium amytal test. (4) Superselective catheterization is performed with the catheter directly abutting the tumor capsule. (5) Particulate, rather than glue-based, embolisate is used.

Pineal region meningiomas are rare, accounting for 0.3% of intracranial meningiomas and 6% to 8% of pineal region tumors.12 These uncommon lesions can draw their blood supply from a variety of sources, including meningeal branches of the ECA, the tentorial artery, medial or lateral posterior choroidal branches, branches of the superior vermian or superior cerebellar artery (SCA), meningeal branches of the posterior inferior cerebellar artery (PICA), or VAs. Sagoh et al. reported successful embolization of a pineal region meningioma with estrogen alcohol and polyvinyl alcohol (PVA) via the bilateral MMAs.13

Optic nerve meningiomas are seldom amenable to endovascular treatment because of the shared blood supply between the tumor and the optic nerve. Terada et al. concluded that if the microcatheter can be positioned distal to the origin of the central retinal artery, embolization is possible. However, the risk of causing blindness is high if reflux occurs into the central retinal artery.14 In many cases, aggressive embolization of optic nerve meningiomas is neither beneficial nor advisable.


The overall risk associated with endovascular embolization of meningiomas is low.18,19 Major complications include stroke, blindness, intratumoral edema, or hemorrhage. Migration of embolic material via reflux or an unappreciated EC-to-IC anastomosis is the most common cause of major morbidity associated with embolization. The neurointerventionalist must have a working knowledge of the highly variable anatomy of EC-to-IC anastomoses and must constantly remain vigilant for the possibility of proximal reflux. Cataclysmic intratumoral swelling follows embolization, particularly if performed with particle embolisates, and can require emergent resection. Our practice is to resect meningiomas the day after embolization. Tumor swelling can sometimes be mitigated by the administration of corticosteroids.

Minor complications occur in as many as 30% of patients and include facial pain, trismus, or both.19 These side effects can be managed symptomatically with corticosteroids or analgesics and are usually self-limited. Rare complications such as cranial nerve damage (thought to be related to occlusion of the vaso vasorum of the cranial nerves), subarachnoid hemorrhage, or retinal embolus have been reported.20,21 Scalp necrosis is a rare but serious complication occasionally associated with embolization of ECA vessels. Several authors recommend preserving the STA as a donor vessel for a free tissue transfer in the event of massive scalp necrosis.22,23

Patients with skull base meningiomas often become symptomatic with some degree of cranial nerve dysfunction. Embolization can exacerbate this dysfunction, which should be emphasized during preoperative patient counseling. Embolization of the petrous branches of the MMA (which frequently supplies lesions of the posterior fossa or posterior parasellar region) can result in damage to the facial nerve. Embolization of branches of the ascending pharyngeal artery (which supplies clival or petroclival meningiomas) risks damage to the lower cranial nerves. The practice of superselection of tumor vessels as distally as possible, ideally with the microcatheter immediately adjacent to the tumor capsule, decreases the risk of inadvertent embolization of vessels supplying normal tissue. If there is any uncertainty, provocative testing may help define the shared vascular supply to the cranial nerves.


Paragangliomas (PGGLs) are typically benign, slow-growing tumors arising from chemoreceptors located in blood vessel walls. Paragangliomas, which are highly vascular tumors, are often referred to a neurointerventionalist for presurgical embolization at the surgeon’s request. In the head and neck, the most common location is at the carotid body, followed by the temporal bone (glomus jugulare or glomus tympanicum) and upper pharyngeal space (glomus vagale). Although histologically similar to pheochromocytomas, only 4% of paragangliomas of the head and neck are associated with catecholamine hypersecretion. Clinical evidence of paroxysmal catecholamine surges must be evaluated preoperatively with 24-hour urine fractionated catecholamine and metanephrine measurements.

Certain familial patterns or association with genetic syndromes (multiple endocrine neoplasia II, neurofibromatosis 1, von Hippel-Lindau (VHL) disease, familial paraganglioma, or Carney triad) have been associated with the diagnosis of paragangliomas. Multiple paragangliomas have been found in 22% and 87% of sporadic and familial paragangliomas, respectively.24,25 Indium-111 octreotide, a radioisotope somatostatin analogue, has been used as a labeling tracer to selectively identify multiple or metastatic paragangliomas.26

Carotid body tumors arise from the carotid body, which is located at the posterior aspect of the carotid bifurcation. The chemoreceptive cells of the carotid body are located in the periadventitia of the carotid bifurcation and are primarily responsive to hypoxia. Conditions of chronic hypoxia, such as living in high altitudes (more than 1500 m above sea level), chronic obstructive pulmonary disease, and cyanotic heart disease are known risk factors for the development of carotid body tumors.

The most common presentation associated with carotid body tumors is a painless, slowly enlarging neck mass. These tumors can cause lower cranial nerve dysfunction (i.e., hoarseness, stridor, or hypoglossal palsy) due to local mass effect, but they rarely grow larger than 4 cm. The diagnosis of carotid body tumors can be confused with glomus vagale. The latter lesions typically arise from paraganglionic tissue rests within the nodose ganglion and are found immediately rostral to the carotid bifurcation. The angiographic appearance of carotid body tumors and glomus vagale tumors differs in that carotid body tumors characteristically splay the ICA and ECA (Fig. 89-2), whereas vagal paragangliomas tend to displace the carotid arteries anteriorly and medially.27

Glomus jugulare tumors arise from glomus rests within the jugular foramen. Patients often complain of progressive unilateral hearing loss or pulse-synchronous tinnitus. Otoscopic examination of the external auditory canal may reveal a red or blue pulsatile mass. If seen on computed tomography (CT), bone-remodeling phenomena (e.g., demineralization, erosion, and destruction of bony structures) can be suggestive of the presence of a paraganglioma within the temporal bone. Gadolinium-enhanced magnetic resonance imaging (MRI) remains the predominant, noninvasive diagnostic imaging modality. On both T1- and T2-weighted sequences, these lesions typically appear as intensely gadolinium-enhancing masses with “salt-and-pepper” flow voids.

Angiography of these lesions must identify the intracranial and extracranial supply to the tumor, as well as the involvement of the dural venous sinus system. The patency of both transverse and sigmoid sinuses must be evaluated to determine whether sacrifice of the involved sinus is feasible without causing venous hypertension and infarction. The blood supply to a carotid body tumor is typically derived from proximal ECA branches or is derived directly from the bifurcation. The blood supply to tympanojugular tumors is almost uniformly derived from the ascending pharyngeal artery.28 Glomus tympanicum tumors usually receive blood supply from the inferior tympanic branch of the ascending pharyngeal artery, while branches of the neuromeningeal trunk supply the hypoglossal canal and jugular fossa lesions. These lesions tend to be small and rarely require preoperative embolization. Glomus tumors within the temporal bone are often fed by branches of the petrous (via the vidian artery) or cavernous (clival branch of the MHT) segments of the ICA.

Glomus jugulare tumors, particularly those that extended into the intracranial compartment, require preoperative embolization.29 These lesions frequently are multicompartmentalized, with a separate arterial supply to each compartment. To achieve complete embolization of a glomus jugulare tumor, the neurointerventionalist must selectively catheterize and embolize each arterial feeding vessel. In general, the ascending pharyngeal artery supplies the inferomedial compartment, while the stylomastoid branch of the occipital or posterior auricular artery contributes to the posterolateral compartment. The anterior compartment tends to be supplied by branches of the internal maxillary artery or the caroticotympanic artery. Branches of the MMA typically feed the superior compartment. If sacrifice of the jugular vein or sigmoid sinus will be necessary, the intracranial venous outflow system should be evaluated during angiography.

Superselective catheterization of the arterial pedicles is crucial for evaluating the angioarchitecture of the tumor and for identifying EC-to-IC anastomoses. Many such superselective microcatheterizations may be required to opacify or embolize the entire tumor. Tumors with substantial supply from the ICA or significant encasement of the ICA may not be amenable to surgical resection and can be evaluated for possible vessel sacrifice with balloon test occlusion.

Embolization reduces operative time and intraoperative blood loss.30,31 In the hands of an experienced neurointerventionalist, the risk of embolization for carotid body tumors is acceptably low, although the yield is probably too low to justify embolization of lesions smaller than 2 cm. Due to local soft-tissue inflammatory response, surgery within 48 hours of embolization is strongly recommended.


Most severe complications associated with embolization of head and neck paragangliomas are related to inadvertent migration of embolisate into the intracranial circulation, either through reflux or through the rich and highly variable EC-to-IC anastomotic network. Embolization of glomus jugulare tumors can cause lower cranial nerve palsies, presumably from embolization of the vaso vasorum supplying these nerves. Facial nerve palsies and even herniation syndromes have also been reported as rare complications of glomus jugulare tumor embolization.32,33 Temporary facial nerve paresis is common after embolization because the facial nerve often receives its blood supply from the stylomastoid artery and the petrosal branches of the MMA or accessory meningeal artery. Recovery of facial nerve paresis is more common when PVA is used as the embolic agent because the vessels tend to recanalize. Provocative testing should be undertaken before glue embolization because this embolisate is relatively permanent and may lead to irreversible deficits.


Hemangioblastomas are benign, hypervascular neoplasms primarily found in the cerebellum or spinal cord. They account for 1% to 2% of craniospinal tumors and occur most commonly within the cerebellar hemispheres, followed by the vermis, cerebellopontine angle, or brain stem.6 Most hemangioblastomas are sporadic, but 20% are associated with VHL disease. The disease has an autosomal dominant inheritance pattern with incomplete penetrance. Multiple hemangioblastomas are common in patients with VHL disease.

Operative morbidity is high because of uncontrollable bleeding, so naturally these lesions have been targeted for preoperative embolization.34 The blood supply to cerebellar hemangioblastomas is typically from PICA, but AICA or SCA branches can also contribute. Pontomedullary lesions often derive their blood supply from SCA branches, while cervicomedullary lesions are supplied by branches of the VA or anterior spinal artery. Superficial lesions can draw blood supply from dural branches of the VA (i.e., posterior meningeal artery). Due to the highly vascular nature of these lesions, the caliber of the feeding artery can exceed that of the basilar artery.

The risk associated with embolization of hemangioblastomas is high because the feeding arteries are often pial vessels. Suboptimal penetration of embolisate into the tumor nidus offers little in terms of reducing operative blood loss, particularly in posterior fossa lesions. The patient is thereby exposed to the risk of the embolization procedure without incurring any benefit.35 Embolization of posterior fossa hemangioblastomas has been associated with complication rates as high as 50%, although some studies have shown preoperative embolization to be a helpful adjunct to resection.36,37 Some authors postulate that postembolization hemorrhage is related to venous outflow obstruction.38,39

Between 1995 and 2009, we successfully embolized 13 posterior fossa hemangioblastomas. One patient suffered a nonfatal complication (stroke) as a result of embolization. Therefore, the morbidity rate was 7.7%. In 3 cases, embolization was aborted due to the lack of tumor vessels suitable for embolization. This underscores one of the tenets of safe embolization of posterior fossa hemangioblastomas: Judicious tumor selection is key to minimizing complications. Only a small percentage of hemangioblastomas resected at our institution are deemed suitable for preoperative embolization. Embolization is reserved for large lesions, lesions with arterial feeders that are difficult to access surgically, or lesions that cannot be resected due to intraoperative hemorrhage. By placing the microcatheter tip beyond normal vessels directly into the tumor vasculature, the risks associated with embolization can be mitigated. PVA and n-butyl cyanoacrylate (n-BCA) are the embolisates of choice for these lesions, although we have successfully used Onyx in two cases.

Clearly, the potential for postembolization hemorrhage or swelling exists and can be especially precipitous in the posterior fossa. However, we strongly believe that by meticulously adhering to the tenets of superselective catheterization and intracranial tumor embolization, hemangioblastomas of the posterior fossa can be safely embolized to aid surgical resection.


Hemangiopericytomas are aggressive tumors arising from the contractile pericytes of Zimmerman, which are leiomyoblastic cells surrounding capillaries and postcapillary venules. These intracranial extra-axial neoplasms account for less than 1% of intracranial tumors. They are associated with high rates of recurrence and have the potential for metastasis.

Hemangiopericytomas are highly vascular lesions, and intraoperative hemorrhage can be significant. Hemorrhage is the most common cause for subtotal resection or operative morbidity. Embolization substantially reduces intraoperative bleeding and facilitates resection.4042 However, embolization can be technically difficult because these tumors tend to parasitize cortical vessels. Ethanol and direct surgical puncture have been successfully employed in the past, although we have had success with Onyx, n-BCA, and PVA. Postembolization swelling is common with these lesions; therefore, resection within 48 hours of embolization is recommended.

Juvenile Nasal Angiofibromas

Juvenile nasal angiofibromas (JNAs) are benign, extremely vascular, nonencapsulated neoplasms consisting of vascular and connective tissue. They usually arise from the superior posterior margin of the sphenopalatine foramen. JNAs are the most common benign tumor of the nasopharynx and account for 0.05% to 0.5% of all head and neck tumors.43 These tumors almost exclusively affect adolescent boys; the mean age at diagnosis is 14 years. JNAs rarely metastasize but display locally malignant behavior and exhibit high rates of recurrence after subtotal resection.44 Approximately 30% of JNAs manifest with intracranial extension.45 The most common presenting symptoms are epistaxis and prolonged nasal obstruction.

The unique appearance of JNAs on CT and MRI eliminates the need for biopsy, which can result in uncontrollable bleeding. Angiography demonstrates multiple tortuous feeding vessels followed by a dense, homogeneous blush in the capillary phase (Fig. 89-3). Prominent draining veins are apparent immediately in the early venous phase. JNAs are typically supplied by branches of the internal maxillary artery, with contributions from the ascending pharyngeal artery in as many as 33% of cases.46 Bilateral carotid angiography is mandatory in all cases, particularly if there is intracranial extension, because these tumors can recruit blood supply from the ophthalmic artery, contralateral internal maxillary artery, and branches of either ICA.

Surgical resection is regarded as the primary treatment modality.47

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